MiR-9-5p promotes M1 cell polarization in osteoarthritis progression by regulating NF-κB and AMPK signaling pathways by targeting SIRT1

巨噬细胞极化 安普克 信号转导 细胞生物学 NF-κB 流式细胞术 癌症研究 污渍 生物 化学 磷酸化 巨噬细胞 分子生物学 体外 基因 蛋白激酶A 生物化学
作者
Jing Wang,Sha Ma,Juan Yu,Dachen Zuo,Xia He,Haiting Peng,Xiaoqing Shi,Weijuan Huang,Qin Li
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:101: 108207-108207 被引量:13
标识
DOI:10.1016/j.intimp.2021.108207
摘要

To investigate the roles and regulatory mechanisms of miR-9-5p in the development of osteoarthritis (OA).Synovial tissues from mouse OA model and control groups were collected and miR-9-5p expression levels and macrophage markers were measured with qPCR. The function of miR-9-5p in macrophage polarization was analyzed by flow cytometry and qPCR. Various databases were employed to screen the target genes one of which was validated with dual-luciferase analysis. Following the validation, rescue research was applied, and the signaling pathways were analyzed with Western blotting. Finally, the role of miR-9-5p in the progression of OA was validated in the mouse model.MiR-9-5p was highly expressed in the synovial tissues of the OA model and was positively associated with M1 markers. Function analysis demonstrated that miR-9-5p could promote the progression of OA by promoting M1 polarization and inhibiting M2 polarization in vivo and in vitro. The mechanism analysis demonstrated that miR-9-5p could regulate macrophage polarization via NF-κB and AMPK signaling pathways by inhibiting SIRT1 expression.MiR-9-5p could promote M1 polarization and OA progression by regulating NF-κB and AMPK signaling pathways by inhibiting SIRT1 expression.
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